Hsp20 Promotes Endothelial Progenitor Cell Angiogenesis via Activation of PI3K/Akt Signaling Pathway Under Hypoxia (Aug, 10.1007/s13770-022-00481-1, 2022)

被引:2
作者
Han, Zhiqi [1 ,2 ,3 ,4 ]
He, Xuan [1 ,2 ,3 ,4 ]
Feng, Yuan [1 ,2 ,3 ,4 ]
Jiang, Weidong [1 ,2 ,3 ,4 ]
Zhou, Nuo [1 ,2 ,3 ,4 ]
Huang, Xuanping [1 ,2 ,3 ,4 ]
机构
[1] Guangxi Med Univ, Nanning 530021, Guangxi, Peoples R China
[2] Guangxi Med Univ, Hosp Stomatol, Dept Oral & Maxillofacial Surg, Coll Stomatol, Nanning 530021, Guangxi, Peoples R China
[3] Guangxi Key Lab Oral & Maxillofacial Surg Dis Tre, Guangxi Key Lab Oral & Maxillofacial Rehabil & Re, Nanning 530021, Guangxi, Peoples R China
[4] Guangxi Clin Res Ctr Craniofacial Deform, Nanning 530021, Guangxi, Peoples R China
基金
中国国家自然科学基金;
关键词
Angiogenesis; Endothelial progenitor cells; Heat shock protein 20; Hypoxia; PI3K/Akt pathway;
D O I
10.1007/s13770-022-00494-w
中图分类号
Q813 [细胞工程];
学科分类号
摘要
Background:: Mandibular distraction osteogenesis (MDO) is a kind of endogenous tissue engineering technology that lengthens the jaw and opens airway so that a patient can breathe safely and comfortably on his or her own. Endothelial progenitor cells (EPCs) are crucial for MDO-related angiogenesis. Moreover, emerging evidence suggests that heat shock protein 20 (Hsp20) modulates angiogenesis under hypoxic conditions. However, the specific role of Hsp20 in EPCs, in the context of MDO, is not yet known. The aim of this study was to explore the expression of Hsp20 during MDO and the effects of Hsp20 on EPCs under hypoxia. Methods:: Mandibular distraction osteogenesis and mandibular bone defect (MBD) canine model were established. The expression of CD34, CD133, HIF-1α, and Hsp20 in callus was detected by immunofluorescence on day 14 after surgery. Canine bone marrow EPCs were cultured, with or without optimal cobalt chloride (CoCl2) concentration. Hypoxic effects, caused by CoCl2, were evaluated by means of the cell cycle, cell apoptosis, transwell cell migration, and tube formation assays. The Hsp20/KDR/PI3K/Akt expression levels were evaluated via immunofluorescence, RT-qPCR, and western blot. Next, EPCs were incorporated with either Hsp20-overexpression or Hsp20-siRNA lentivirus. The resulting effects were evaluated as described above. Results:: CD34, CD133, HIF-1α, and Hsp20 were displayed more positive in the callus of MDO compared with MBD. In addition, hypoxic conditions, generated by 0.1 mM CoCl2, in canine EPCs, accelerated cell proliferation, migration, tube formation, and Hsp20 expression. Hsp20 overexpression in EPCs significantly stimulated cell proliferation, migration, and tube formation, whereas Hsp20 inhibition produced the opposite effect. Additionally, the molecular mechanism was partly dependent on the KDR/PI3K/Akt pathway. Conclusion:: In summary, herein, we present a novel mechanism of Hsp20-mediated regulation of canine EPCs via Akt activation in a hypoxic microenvironment. © 2022, Korean Tissue Engineering and Regenerative Medicine Society.
引用
收藏
页码:1389 / 1390
页数:2
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[1]  
Han ZQ, 2022, TISSUE ENG REGEN MED, V19, P1251, DOI 10.1007/s13770-022-00481-1